Abstract
Ca2+ is essential for virus entry, viral gene replication, virion maturation, and release. The alteration of host cells Ca2+ homeostasis is one of the strategies that viruses use to modulate host cells signal transduction mechanisms in their favor. Host calcium-permeable channels and pumps (including voltage-gated calcium channels, store-operated channels, receptor-operated channels, transient receptor potential ion channels, and Ca2+-ATPase) mediate Ca2+ across the plasma membrane or subcellular organelles, modulating intracellular free Ca2+. Therefore, these Ca2+ channels or pumps present important aspects of viral pathogenesis and virus–host interaction. It has been reported that viruses hijack host calcium channels or pumps, disturbing the cellular homeostatic balance of Ca2+. Such a disturbance benefits virus lifecycles while inducing host cells’ morbidity. Evidence has emerged that pharmacologically targeting the calcium channel or calcium release from the endoplasmic reticulum (ER) can obstruct virus lifecycles. Impeding virus-induced abnormal intracellular Ca2+ homeostasis is becoming a useful strategy in the development of potent antiviral drugs. In this present review, the recent identified cellular calcium channels and pumps as targets for virus attack are emphasized.
Highlights
Viruses exploit the environment of host cells to replicate, thereby inducing host cells’ dysfunction.Virus–host interaction is the foundation of pathogenesis and closely associated with disease severity and incidence
Human cytomegalovirus (HCMV) UL37x1 protein interacts with the host P2Y2 purinergic receptor to increase intracellular Ca2+ levels via the PLC–IP3 pathway, and this activity is important to viral replication [61]
The results obtained from a genome-wide knockout screen indicated that SPCA1 in the Golgi network is critical for human respiratory syncytial virus (RSV) infection [69,70,71]
Summary
Viruses exploit the environment of host cells to replicate, thereby inducing host cells’ dysfunction. Ca2+ -ATPase (SERCA)) and the Na+ /Ca2+ exchanger (NCX) are responsible for transporting Ca2+ from the cytosol to external medium or into cellular calcium stores (red arrows) Viruses utilize these calcium components to elevate cytosolic calcium concentration to activate Ca2+ -dependent/sensitive enzymes and transcriptional factors to promote virus replication (right panel). They utilize various calcium channels and pumps to obviate the cell membrane barriers, enter the host cell, complete replication, acquire infection ability, and release. The research work done on four distinct hemorrhagic fever viruses (Ebolavirus (EBOV), Marburgvirus (MARV), Lassa Virus (LASV), and Junín Virus (JUNV)) demonstrated that EBOV, MARV VP40, and JUNV Z proteins trigger host cell Ca2+ signals by activating the ER Ca2+ sensing protein STIM1 and the plasma membrane ORAI1 channel. Host Transient Receptor Potential (TRP) Channels and Receptor-Operated Calcium (ROC) Channels
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